| Literature DB >> 31591516 |
Javier Gutierrez-Achury1, Ana Florencia Costa2, Patrick Deelen1, Julio Cesar Bai2, Vinod Kumar1,3, Cisca Wijmenga4,5, Isis Ricaño-Ponce1, Alexander Kurilshikov1, Maria Magdalena Zorro1, Mathieu Platteel1, Adriaan van der Graaf1, Serena Sanna1, Oscar Daffra6, Alexandra Zhernakova1, Jingyuan Fu7, Gosia Trynka8, Edgardo Smecuol2, Sonia Isabel Niveloni2.
Abstract
Celiac disease (CeD) is a common immune-mediated disease of the small intestine that is triggered by exposure to dietary gluten. While the HLA locus plays a major role in disease susceptibility, 39 non-HLA loci were also identified in a study of 24,269 individuals. We now build on this earlier study by adding 4125 additional Caucasian samples including an Argentinian cohort. In doing so, we not only confirm the previous associations, we also identify two novel independent genome-wide significant associations at loci: 12p13.31 and 22q13.1. By applying a genomics approach and differential expression analysis in CeD intestinal biopsies, we prioritize potential causal genes at these novel loci, including LTBR, CYTH4, and RAC2. Nineteen prioritized causal genes are overlapping known drug targets. Pathway enrichment analysis and expression of these genes in CeD biopsies suggest that they have roles in regulating multiple pathways such as the tumor necrosis factor (TNF) mediated signaling pathway and positive regulation of I-κB kinase/NF-κB signaling.Entities:
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Year: 2019 PMID: 31591516 PMCID: PMC7028987 DOI: 10.1038/s41431-019-0520-4
Source DB: PubMed Journal: Eur J Hum Genet ISSN: 1018-4813 Impact factor: 4.246